during WD. One possible explanation is that extrasynaptic KAR, and not the synaptic receptors measured in Figure 1, are responsible for ATPA-induced plasticity. However, the initiation of synaptic plasticity at EC-BLA synapses by low-frequency electrical stimulation is dependent on synaptic activation of kainate receptors; and, this process parallels to ATPA-induced plasticity in this same brain region (Li et al., 2001). An alternative explanation is that KAR may be important only for the initiation of the synaptic plasticity at some undefined point during the chronic intermittent ethanol exposure. Regardless, we have recently shown that AMPA receptors are functionally up-regulated during both CIE and WD as well (Lack et al., 2007). Since AMPA receptors have been shown to maintain both NMDAR-dependent and NMDAR-independent LTP in the hippocampus (Grover, 1998) and in the BLA (Maren, 2005; McKernan and Shinnick-Gallagher, 1997; Rogan et al., 1997), our findings suggest that chronic intermittent ethanol engages the mechanisms related to the expression/maintenance of synaptic plasticity, ultimately resulting in the occlusion of ATPA-induced plasticity at the time of our measures. This hypothesis parallels previous findings showing repeated ethanol/withdrawal leading to the occlusion of NMDA-dependent forms of synaptic plasticity in the basolateral amygdala (Stephens et al., 2005).
